miR-137 prevents inflammatory response, oxidative stress, neuronal injury and cognitive impairment via blockade of <i>Src</i>-mediated MAPK signaling pathway in ischemic stroke

Runhui Tian; Bo Wu; Cong Fu; Kaimin Guo

doi:doi:10.18632/aging.103301

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This article is currently undergoing investigation.

Research Paper Volume 12, Issue 11 pp 10873—10895

miR-137 prevents inflammatory response, oxidative stress, neuronal injury and cognitive impairment via blockade of Src-mediated MAPK signaling pathway in ischemic stroke

Figure 11. Downregulated miR-137 activates the MAPK signaling pathway and increases cell apoptosis by increasing Src expression. (A) ERK1/2, p38 and Src in the brain tissues of miR-137^-/- mice by immunohistochemistry (× 200); (B) immunofluorescence images of cleaved caspase 3, TUNEL staining, and DAPI staining in brain tissues from miR-137^-/- mice (× 400); (C) mRNA levels of Erk2, Jnk, p38, Gfap, Bax and Bcl-2 in brain tissues from miR-137^-/- mice detected using RT-qPCR; (D) protein levels of GFAP, Bax and Bcl-2 along with the extent of ERK1/2, JNK and p38 phosphorylation in brain tissues from miR-137^-/- mice detected using Western blot analysis. Measurement data are expressed as mean ± standard deviation and compared using one-way ANOVA, followed by Tukey's post hoc test. * p < 0.05 vs. control group (sham-operated wild-type mice); # p < 0.05 vs. MCAO group (wild-type mouse models of MCAO). N = 15.